Stress and Insufficient Nutrition Program Abnormal Growth of the Embryo

Abstract

Stress and insufficient nutrition in fetal life impose a risk of low birth weight (LBW) and increased vulnerability for chronic childhood and adult diseases. Using a unique avian embryo model, we reported previously that impaired nutrition caused LBW and, after maturation, a low number of nephrons and glomerular mesangium lesions partly resembling nephrosclerosis. In the present study, we determined in Japanese quail, Coturnix japonica, whether the stress imposed on the embryo during the early period of development induces structural defect, whereas insufficient nutrition causes impaired growth and maturation. We also examined whether α‐smooth muscle actin (α‐SMA) may serve as an injury/inflammation marker in glomerular mesangium. We found: 1) At embryonic day 8–9 (E8–9), 45.1% (n = 31) of embryos derived from eggs in which 10% of the egg‐white was withdrawn (EwW) before the start of incubation showed abnormal growth, malformation, and/or early death. At E15–16 (hatch, E17) the rate of abnormal growth/structure was lower (26.4%, n = 34). 2) The weight of the EwW embryos that showed good growth (0.74 ± 0.03 g, n = 8) was not significantly different from that of controls (CT, 0.79 ± 0.02 g, n = 14) at E8–E9, but it was lower (P < 0.01) at E16 (CT, 5.9 ± 0.2 g, n = 13; EwW, 5.2 ± 0.1 g, n = 14). 3) α‐SMA signals were present in renal arteries and arterioles, glomerular mesangium, and peritubular capillaries of embryonic kidneys. α‐SMA signals were stronger in EwW groups both in E16 embryos and in hatched quail. These results suggest that partial withdrawal of egg‐white (92% is protein) before incubation induces structural defect, possibly due to mechanical stress of egg‐white withdrawal (gentle suction via G18 blunt needle), whereas the effect of low nutrition was more obvious in the later embryonic period. α‐SMA in glomerular mesangium may serve as an injury‐inflammation marker in quail kidneys.